Establishment of ventral cell fates in the Drosophila embryonic ectoderm requires DER, the EGF receptor homolog.

The embryonic ectoderm in Drosophila displays a highly organized arrangement of specific structures along the dorsal-ventral axis. To establish this characteristic design, cells must receive instructive cues regarding their position. We present evidence that during stages 8-9 of embryonic development, the Drosophila EGF receptor homolog (DER) is essential for determining the identity of cells within the ventral ectoderm. In the absence of DER activity at this phase, alterations in cell fate are observed: Ventral cells acquire more dorsal fates, as visualized by the expression profile of specific markers. The ventralizing effect of DER appears to function later than that of the dorsalizing dpp pathway, and the spatial overlap between them is minimal. A model for the determination of cell fates along the dorsal-ventral axis involving the two pathways is presented. Some aspects of the mutant ectodermal and CNS phenotypes of the DER locus (faint little ball, flb) resemble the phenotype of mutations from the spitz group. Synergistic interactions between flb and spitz or Star mutations suggest that these genes participate in a common signaling pathway.